Research suggests that Mercury from Silver Dental Fillings may cause Depression, Excessive Anger, and Anxiety.

How is this possible you ask? The study suggests that amalgam mercury may play a role in the cause of depression, excessive anger, and anxiety because mercury can produce such symptoms perhaps by affecting the neurotransmitters in the brain.

Scores on the Beck Depression Inventory were compared for 25 women who had silver dental fillings (amalgams) and for 23 women without amalgams. Women with amalgams had significantly higher scores and reported more symptoms of fatigue and insomnia. Anger scores from the State-Trait Anger Expression Inventory showed that the women with amalgams had statistically significantly higher mean scores on expressing anger without provocation and experiencing more intense angry feelings. The women without amalgams scored significantly higher on controlling anger, which suggested they invested more energy in monitoring and preventing the experience and expression of anger. Anxiety scores from the State-Trait Anxiety Inventory showed the women with amalgams scored significantly less pleasant, satisfied, happy, secure, and steady, and had a more difficult time making decisions. They had significantly higher Trait Anxiety scores. The women with amalgams also had significantly higher levels of mercury in the oral cavity before and after chewing gum. The study suggests that amalgam mercury may be an etiological (cause of) factor in depression, excessive anger, and anxiety because mercury can produce such symptoms perhaps by affecting the neurotransmitters in the brain.

Author: Siblerud RL; Motl J; Kienholz E

Comments

There is definitely more than enough evidence to show the toxicity effects mercury has on the brain and the central nervous system. I believe that Mercury actually physically deteriorate nerve tissues and it causes more than just a neurtransmitter embalance. Mercury destroys brain tissue and nerves and can reproduce the signs and symptoms of many degenerative neurological diseases such as MS and Alzheimer’s Disease. There is a great video ( http://movies.commons.ucalgary.ca/mercury/ ) where you can actually see how ions of Mercury (minute amounts) shrink the nerves growing in a petri dish. So is chronic neurological illness on the rise or is Mercury toxicity to blame? Please tell us your opinion on our blog https://floreshealth.wordpress.com/

July 14, 2011 (Gainesville, Florida)— Older patients with hypertension and coronary artery disease who use nonsteroidal anti-inflammatory drugs (NSAIDs) chronically for pain are at significantly increased risk of cardiovascular events, a new post hoc analysis from the International Verapamil-Trandolapril Study (INVEST) demonstrates [1]. The research is published in the July 2011 issue of the American Journal of Medicine.

“We found a significant increase in adverse cardiovascular outcomes, primary driven by an increase in cardiovascular mortality,” lead author Dr Anthony A Bavry(University of Florida, Gainesville) told heartwire. “This is not the first study to show there is potential harm with these agents, but I think it further solidifies that concern.”

He says the observational study, conducted within the hypertension trial INVEST, is particularly relevant to everyday practice because the patients included were typical of those seen in internal-medicine, geriatric, and cardiology clinics–they were older, with hypertension and clinically stable CAD.

Bavry and colleagues were not able to differentiate between NSAIDs in the study–most people were taking ibuprofen, naproxen, or celecoxib–and he says until further work is done, he considers the risks of NSAIDs “a class effect,” and their use should be avoided wherever possible.

I try to get them to switch to an alternative agent, such as acetaminophen.

However, “Patients should not terminate these medicines on their own,” he says. “They should have a discussion with their physician. When I see patients like these taking NSAIDs I will have an informed discussion with them and tell them there is evidence that these agents may be associated with harm. I try to get them to switch to an alternative agent, such as acetaminophen, or if that’s not possible I at least try to get them to reduce the dose of NSAID or the frequency of dosing. But ultimately, it’s up to them if this potential risk is worth taking depending upon the indication for their use.”

Chronic NSAID Use More Than Doubles CV Mortality

Within the large cohort of more than 22 000 patients in INVEST, Bavry and colleagues identified patients who reported taking NSAIDs at every follow-up visit and termed them chronic users (n=882). Most often, patients were taking these agents for conditions such as rheumatoid arthritis, osteoarthritis, and lower back pain, Bavry said.

They compared the chronic NSAID users with those who only intermittently (n=7286) or never (n=14 408) used NSAIDs over an average of 2.7 years and adjusted the findings for potential confounders.

The primary outcome–a composite of all-cause death, nonfatal MI, or nonfatal stroke–occurred at a rate of 4.4 events per 100 patient-years in the chronic-NSAID group vs 3.7 events per 100 patient-years in the nonchronic group (adjusted hazard ratio 1.47; p=0.0003).

As noted by Bavry, the end point was primarily driven by a more than doubling in the risk of death from CV causes in the chronic-NSAID group compared with never or infrequent users (adjusted HR 2.26; p<0.0001).

The association did not appear to be due to elevated blood pressure, the researchers say, because chronic NSAID users actually had slightly lower on-treatment BP over the follow-up period.

They note that a recent American Geriatrics Society panel on the treatment of chronic pain in the elderly recommends acetaminophen as a first-line agent and suggests that nonselective NSAIDs or COX-2 inhibitors be used only with extreme caution. “Our findings support this recommendation,” they state.

Bavry added: “We do need more studies to further characterize the risks of these agents, which are widely used and widely available, and perhaps the risks are underappreciated. We are working on the next level of studies to try to identify which are the most harmful agents.”

Comments

The majority of my patients taking NSAIDs on a regular basis for a prolonged amount of time take them to deal with muscle aches and joints. The warning I give to them – take them with food since they tend to upset your stomach especially if you have gastritis. I’m curious to know how long researchers knew about this information relating to NSAIDs? How many people have suffered or have even died because of this? The message I would like to leave you with – we have to remember that all drugs have an effect on the body, good and bad. When we neglect to treat the source of any pain or inflammation, and instead treat only the symptoms, it sometimes comes with a very high tag price. ~ Dr. Luis Flores

ScienceDaily (Jan. 6, 2009) — A new epidemiological study has found that among women who have never used menopausal hormone therapy, obese women are at an increased risk of developing ovarian cancer compared with women of normal weight. The research indicates that obesity may contribute to the development of ovarian cancer through a hormonal mechanism.

Ovarian cancer is the most fatal of gynecologic malignancies, and has a 5-year survival rate of only 37 percent. While studies have linked excess body weight to higher risks of certain cancers, little is known about the relationship between body mass index and ovarian cancer risk.

To investigate this issue, Dr. Michael F. Leitzmann of the National Cancer Institute and colleagues studied 94,525 U.S. women aged 50 to 71 years over a period of seven years. The researchers documented 303 ovarian cancer cases during this time and noted that among women who had never taken hormones after menopause, obesity was associated with an almost 80 percent higher risk of ovarian cancer. In contrast, no link between body weight and ovarian cancer was evident for women who had ever used menopausal hormone therapy.

According to Dr. Leitzmann, these findings support the hypothesis that obesity may enhance ovarian cancer risk in part through its hormonal effects. Excess body mass in postmenopausal women leads to an increased production of estrogen, which in turn may stimulate the growth of ovarian cells and play a role in the development of ovarian cancer.

Among women with no family history of ovarian cancer, obesity and increased ovarian cancer risk were also linked in this study. However, women that did have a positive family history of ovarian cancer showed no association between body mass and ovarian cancer risk.

These latest findings provide important additional information related to women’s risks of developing ovarian cancer. “The observed relations between obesity and ovarian cancer risk have relevance for public health programs aimed at reducing obesity in the population,” the authors wrote.

Comments

There is more and more evidence pointing out hormonal activity of fat in the body and therefore it is no surprise that there is a direct link between increased body fat and ovarian cancer which is a hormone driven cancer. It is well known that obesity and increased abdominal weight is becoming an epidemic in our society in all age groups and many chronic illnesses are on the rise because of this. Lifestyle and optimal nutrition are key factors that can prevent weight gain and therefore reduce risk of many prevalent chronic illnesses including cancer. Flores Health Services is having a friends/family day every last Wednesday of the month where we give 50% off an initial visit to your friends and family. Our team at Flores Health Services looks forward to helping you and your family reach your health goals.

Maternal exposure to compounds present in crude oil, cleaning agents, and
stain removers has been linked to an increased risk for congenital heart
disease (CHD) in a study presented here at the Pediatric Academic Societies
and Asian Society for Pediatric Research 2011 Annual Meeting.

CHD “is a major cause of childhood death and life-long health problems, so
identifying risk factors contributing to CHD is important to public health.
Environmental causes of CHD have been suspected, and animal studies have
linked certain chemicals to CHD as potential teratogens, but the link has
remained unproven,” Gail McCarver, MD, professor of pediatrics at the
Medical College of Wisconsin and Children’s Research Institute, Milwaukee,
told Medscape Medical News.
To probe whether human exposure to a battery of volatile organic compounds
and halogens increased the risk for CHD, Dr. McCarver and her colleagues
tested meconium as a means of assessing fetal exposure to the solvents.

“Meconium monitoring is an established and valid means of assessment of
fetal exposure,” Dr. McCarver noted in an interview with Medscape Medical
News.

Meconium from 135 newborns diagnosed with CHD and 432 newborns without
CHD, as determined by echocardiography, was examined for 17 compounds using
gas chromatography–mass spectrometry for volatile organic compounds and gas
chromatography–electron capture detector for halogens.

Both techniques were exquisitely sensitive, with detection limits in the
parts-per-trillion range.

Infants of diabetic mothers and infants identified with chromosomal
abnormalities linked to CHD were excluded from the study. Demographic data,
information concerning family history of CHD, and maternal history of the
use of tobacco, alcohol, illicit drugs, and vitamins were collected. Mothers
and infants were genotyped for 2 genes implicated in CHD: ADH, which
encodes alcohol dehydrogenase, and CYP2E1, which encodes cytochrome
P450 2E1.

The infants with CHD were significantly more likely to be smaller at birth,
born at an earlier gestational age, white, have a family history of CHD, and
born to a woman who smoked tobacco (P < .05 for all).

When the data were examined on the basis of race, fetal exposure to ethyl
benzene (a component of crude oil) and the inhaled vapors of vehicle
emissions, gasoline, and cigarette smoke increased the risk for CHD 4-fold
in white infants, but not in black infants. Exposure to trichloroethylene (a
common degreasing chemical that is a component of a variety of cleaners and
spot removers) increased CHD risk 2-fold in white infants and 8-fold in
black infants.

Maternal obesity; tobacco smoking; the use of alcohol, illicit drugs, or
vitamins; exposure to other solvents; and presence/absence of ADH and
CYP2E1 were not significant CHD risk factors.

The association between ethylbenzene and CHD — described by Dr. McCarver as
“novel and important for public health” — might explain previous reports
linking smoking during pregnancy and CHD, and might heighten public health
concerns about events such as the recent oil spill in the Gulf of Mexico.

“This is the first report that exposure to ethyl benzene, a compound present
in crude oil, is associated with CHD. This association is troubling,
particularly concerning recent oil spills,” Dr. McCarver told Medscape
Medical News.

The data also implicate tetrachloroethylene as a teratogen and strengthen
the validity of the noninvasive examination of meconium as a means of
analyzing fetal exposure to environmental compounds.

“This is valuable work. But it could, perhaps, be a whole bunch more
insightful if we had more of a history of maternal exposure and its relation
to pregnancy. This would allow a more accurate assessment of exposure as a
causal factor,” Robert Geller, MD, from Emory University School of Medicine,
Atlanta, Georgia, told Medscape Medical News.Dr Flores’ comments:

There is more and more evidence of the deleterious effects of environmental toxins on human health. Although this study is with infants, there must be similar effects seen in other apparently healthy individuals that don’t show any immediate symptoms. The affect of all of these man made toxins is without a doubt an issue that we will be hearing more often as the cause of many diseases. Detoxifying on regular basis is a great way to combat these environmental toxins and their effects on human health. The only way to protect ourselves and our family from the deleterious effects of all of these non fat soluble toxins and even from electrosmog is to avoid exposure as much as possible, and to focus much more on detoxification. One of the primary treatments that we offer at Flores Health Services is Lymphatic Drainage – when paired with customized homeopathic detoxification remedies this is a way to boost your bodies ability to rid itself of toxic build up that we are faced with on a daily basis.

The incidences of full-blown celiac disease increased by 400 percent in the last 50 years!

SOMETHING YOU’RE EATING may be killing you, and you probably don’t even know it! If you eat cheeseburgers or French fries all the time or drink six sodas a day, you likely know you are shortening your life. But eating a nice dark, crunchy slice of whole wheat bread–how could that be bad for you? Well, bread contains gluten, a protein found in wheat, barley, rye, spelt, kamut, and oats. It is hidden in pizza, pasta, bread, wraps, rolls, and most processed foods. Clearly, gluten is a staple of the American diet. What most people don’t know is that gluten can cause serious health complications for many. You may be at risk even if you don’t have full blown celiac disease. I want to reveal the truth about gluten, explain the dangers, and provide you with a simple system that will help you determine whether or not gluten is a problem for you.

The Elimination/Reintegration Diet
While testing can help identify gluten sensivity, the only way you will know if this is really a problem for you is to eliminate all gluten for a short period of time (2 to 4 weeks) and see how you feel. Get rid of the following foods:
• Gluten (barley, rye, oats, spelt, kamut, wheat, triticale–see www.celiac.com for a complete list of foods that contain gluten, as well as often surprising and hidden sources of gluten.)
• Hidden sources (soup mixes, salad dressings, sauces, as well as lipstick, certain vitamins, medications, stamps and envelopes you have to lick, and even Play-Doh.)
For this test to work you MUST eliminate 100 percent of the gluten from your diet–no exceptions, no hidden gluten, and not a single crumb of bread.
Then eat it again and see what happens. If you feel bad at all, you need to stay off gluten permanently. This will teach you better than any test about the impact gluten has on your body.

WINDSOR, Ont. – Women who work in the home are at a 54 percent higher risk of developing cancer than women who work outside the home, according to Michael Dufresne, a leading researcher in environmental cancers.

Women and men who want to look good and avoid body odours are at added risk, because of the cancer causing chemicals in hundreds of personal care products and household cleaners, said Dufresne, quoting from leading studies.

From cosmetics and hair products to toothpaste, shaving cream, furniture polish, and dish washing liquid, the presence of cancer-linked chemicals raises major concern, said Dufresne, a research professor at the University of Windsor, who is also a research coordinator for Cancer Care Ontario and a member of the U.S. Barbara Karmanos Cancer Institute.

Speaking at a seminar here Tuesday, Dufresne said his greatest worry is the lack of information given to the public about products they use every day.

“People are blindly being led in the use of these products, they assume they are tested and safe, and they’re not,” said Dufresne. “Scientists are discovering that exposure to a variety of trace chemicals over the span of a lifetime is dangerous.”

An estimated 68,600 Canadian woman will be diagnosed with cancer this year, while 31,600 of them will die. Forty-six percent of Canadian woman are in the workforce and the remainder work at home.

The U.S. Public Interest Group reports there are more than 100,000 synthetic chemicals in use. Residues of more than 400 toxic chemicals have been identified in human blood and fat tissues.

The risk of childhood leukemia and brain tumours increases dramatically in households using home an garden pesticides, herbicides, and insecticides. Bleach is being linked to the rising rates of breast cancer.

Dufresne said the biggest culprit is the cosmetic industry, which does not put warnings on labels and does not list potentially harmful ingredients. “The industry and the regulators know the cancer risks associated with cosmetics but there is virtually no consumer knowledge,” Dufresne said, “Unlike cigarettes, there are no warning labels on cosmetics and virtually no FDA regulations policing them.

Cancer-linked chemicals are found in blush, concealer, facial powder, mascara and eye shadow and lipstick.

The amount of insulin within the body determines the amount of fat-maker message. Hormones, like insulin, carry information to the body cells. Hormone information always concerns how cells direct energy expenditure. Insulin carries information that tells the cells to store energy. Most body energy storage occurs as fat. Cholesterol is one type of body fat. The enzyme in the liver that makes sugar into cholesterol turns up its activity when insulin levels rise. Insulin levels rise following carbohydrate meals or excess mental stress (among several other promoters). Rather than tell doctors and the public about this simple cause and effect relationship, the wonders of the statin drugs bombards media outlets.

Statin drugs work, in part, because they poison this liver enzyme’s ability to listen to the insulin message. The trouble with poisons concerns their inevitable side effects and toxicities. One nasty side effect from these medications concerns the depletion of Co enzyme Q10 in the body. The heart needs the lion’s share of this important nutrient. Deficiency here causes one type of heart failure.

Another emerging understanding for how stain drugs lower heart disease risk involves their ability to subdue inflammation. Rather than come clean and educate physicians about the most likely mechanism for how this occurs, the statin-selling companies perpetrate the story that it remains largely a mystery. The argument for it being a mystery diminishes once a few critical clues enter into the discussion.

The first clue involves the long-known association between heart disease and the Type A personality types. Type A personality types are classically described as hard driving, over achieving, and always worried about their next deal. Physiologically, these emotions when chronically expressed, lead to a constant stress hormone response. The stress response was designed to survive physical stressors. In order to survive a physical stress, the massive dumping of fuel into the bloodstream makes sense because exercising muscles consume the fuel. Additionally, physical stressors often lead to trauma. This explains why the acute phase reactants predictably elevate with the onset of the stressor. The acute phase reactants prove appropriate with trauma, but deleterious with mental stress. C-reactive protein is only one acute phase reactants prove appropriate with trauma, but deleterious with mental stress. C-reactive protein is only one acute phase reactant. Others include complement, interferon, fibrinogen, ferritin, ceruloplasmin and amyloid. Fibrinogen directly increases the clotting tendencies of blood. Ferritin elevations increase iron absorption into the body tissues.

With mental stress, once iron absorbs into the body, it proves very difficult to remove. This detail may help explain the emerging realization that many heart disease patients have elevated ferritin levels. It further explains a potential reason that chelation therapy maintains its devotees, despite the ongoing criticism. Specifically, EDTA binds and removes iron from the body. This fact may prove the number one benefit for this approach.

Lastly, concerning the acute phase reactants’ elevation in the setting of mental stressors, involves its inappropriate effects toward an increase in angiogenesis propensity. The angiogenesis propensity increases when the acute phase reactants elevate. This again makes sense with physical stressors because these traumas associate with the need for new blood vessel formation.

Chronic mental stress promotes two powerful processes that promote the angiogenesis critical to tumor growth: increased insulin needs and the heightened angiogenesis propensity described above. These facts, taken together, provide a likely mechanism for why overweight and stressed individuals suffer increased morbidity and mortality from cancer.

The second clue involves the emerging research results that document that the statin drugs lower C-reactive protein levels. Once one recalls the connection between HMG Co A reductase activity and steroid synthesis rates, a more holistic picture emerges. Anything that subdues the ability of the adrenal glands to make steroids, will also diminish the magnitude of cortisol released for a given stressor. In turn, less coritsol release subdues the acute phase reactants, in the chronic mentally stressed state, leads to less inflammation for the reasons described above.

These facts initially sound “too good to be true.” This old adage once again proves useful because the downside to this scenario provides insight into the advantages of counseling Type A personality owners about the bigger picture of cause and effect relationships.

In order to better appreciate the downside of the statins, one needs to recall typical body habitus of the Type A personality. The majority of them are large in the waistline, or at the very least, they have increased visceral fat. Currently, a waist measurement above 40 inches is felt to predict these metabolic syndrome types at risk for accelerated aging and blood vessel disease. Over fifty years ago, obese individuals were found to have increased stress steroid metabolites in their urine.

Uniting these two facts together, it becomes easier to understand one of the metabolic syndrome individual’s driving pathological forces: Exaggerated stress steroid release rate for a given stressor. Another way to look at this is, in the setting of chronic mental stress, those prehistorically-equipped survival machines selected for down through the ages have become the metabolic syndrome victims from chronic sedentary-type stressors. What was once a survival benefit derived from mounting a strong fuel release and acute phase reactant release (both secondary to a strong cortisol release) in the setting of physical stress, has now become a curse, promoting excessive body fat accumulation and blood vessel inflammation.

Excessive cortisol release violently activates protein dismantling into more sugar (gluconeogenesis). Protein content within denotes the metabolically active constituent of body tissue. Defense of body protein content proves fundamental to healthful longevity. Healthy people have sufficient growth hormone release that protects their protein from excessive catabolism during these times. However, middle-aged individuals who chronically experience stress but have sedentary lifestyles, begin to suffer various amounts of glandular decline.

One mechanism for glandular decline involves the inappropriate elevation of blood sugar caused by mental stress in the sedentary state. Elevated blood sugar suppresses growth hormone release. Less growth hormone release leads to less defense of body protein ability. This fact ties in the observation about syndrome X patients evidencing sarcopenia. It also elucidates the likely association between this Syndrome, and its underlying a variant presentation of Cushing’s disease pathology (see testing below).

With mental stress, the increased blood fuel has nowhere to go. Hence, for these reasons, increased insulin amounts eventually release to normalize the blood sugar. Again, this same metabolic derangement operates within the classical Cushing’s disease patient. Unfortunately, very few physicians appreciate the sequential release of first cortisol (catabolic) followed by increased need for insulin to correct the inappropriate rise in blood sugar. It is the increased insulin that makes the typical Cushing’s disease patient fat. It is the increased cortisol that causes excessive catabolism of their body protein and chronic surges in their blood sugar levels.

Unfortunately, insulin releases into the portal vein and heads straight for the liver. HMG Co A reductase turns on with increasing insulin and off with increasing glucagons. What was once protein, a few minutes before, now is floating within the bloodstream as sugar. A few minutes later the protein turned into sugar is changed into cholesterol and fat. Because the liver (also fat cells) cells have 200,000 pure insulin-type receptors per cell, insulin excess profoundly influences the cholesterol profile.

A cognizance of this anatomical reality helps one to see that the liver functions as an insulin trap and only excessive amounts of insulin secretion can spill past the liver and out into the general circulation. Healthy people need less insulin because their livers secrete sufficient IGF-1 that largely negates the need for insulin between meals, while fasting or when exercising. Circulating IGF-1 levels directly depend on sufficient growth hormone release. Realize, only sufficient growth hormone release defends body protein between meals, while exercising or when fasting. All other counter-regulatory hormones (cortisol, epinephrine and glucagon) make protein dismantling for fuel creating fair game.

The old name for IFG-1 clarifies its crucial role in sugar metabolism, the nonsuppressible insulin-like activity of the bloodstream. Many physicians remain unaware of this fact and it seems rather odd to this author that it fails to receive even cursory mention while reviewing Syndrome X pathology. The healthiest people possess the highest IGF-1 levels. A falling IGF-1 leads to increased insulin need (insulin resistance).

The very survival of the statin drug-selling rosy picture depends on eviscerating certain scientific consequences that result from a diminished glandular ability. When healthy, the adrenal glands make both catabolic and anabolic message content. A higher anabolic message content leads to a faster repair rate. The lower the antioxidants, the more repairs need to occur. Here lies the additional risk of chronically consuming statin drugs in place of healing lifestyles: They contribute to the lack of repair from ongoing wear and tear that the blood vessels encounter. Disrepair causes inflammatory damage despite their benefit from inducing decreased cholesterol and acute phase reactants levels.

HMG Co A reductase occurs within the adrenals and gonads. Any drug or toxin that inhibits the steroid manufacture ability within the adrenals or gonads, will also decrease the repair rate that logically follows from diminished anabolic message content. Here lies another downside that remains ignored until one begins to examine the interrelatedness of steroid synthesis rates and HMG Co A reductase activity.

In one way or another, blood vessel disease results from the repair rate not keeping up with the injury rate. Statin drugs may in fact lower the injury rate by diminishing the acute phase reactants’ caused inflammation and cortisol-related blood sugar spikes. The lessened blood sugar spikes lead to decreased insulin need despite a sedentary and stress-filled lifestyle. A subdued stress response means that less acute phase reactants release, as well. However, what is not being said concerns their probable negative influence on the repair rate of blood vessels and muscle tissue. The repair rate of muscles and blood vessels depend on androgen levels, like all other DNA-containing body cells. Since science has already documented subdued acute phase reactants with statin usage, it remains quite likely that other steroids’ synthesis rates decrease, as well.

The likely consequence of diminished testosterone, which results from statin drug usage, may help further elucidate the ongoing suspicion about their contribution to heart failure. Many in the holistic community attribute this tendency to the diminished Coenzyme Q10 levels that logically follow. However, maybe a fall off in testosterone in some chronic statin users, contributes to their pump failure as well.

Following serial 24-hour urine measurements for steroids would provide a logical next step for testing the severity of diminished anabolic message content. It will also further elucidate the before and after profiles of the stress steroid metabolites of Syndrome X patients. Recall, that over 50 years ago, obese patients were documented to have elevations in their 24-hour urine test for stress steroid metabolites. If each doctor in the holistic community began collecting baseline 24-hour urine specimens for steroids, and followed them serially, a new level of understanding would emerge about the association of a heightened stress response, increased insulin need, and elevated acute phase reactants in the development of blood vessel disease. At the very least, real hormone replacement therapy could be instituted to address these steroid defects before they weaken the statin drug user. Ideally, these types of tests could be used to help better motivate the type A personality – derived Syndrome X individual take a more active role in which hormones secrete.